Publication: Altered ratio of proapoptotic and antiapoptotic proteinsin different brain regions of female rats in modelof post-traumatic stress disorder
Abstract
B-hücre lenfoma/lösemi-2 (Bcl-2) protein ailesi, proapoptotik (Bax) ve antiapoptotik (Bcl-2) proteinleri arasındaki denge ile kontrol edilen programlı hücre ölümü işleminde mitokondri zar geçirgenliğini düzenlemektedir. Post travmatik stress sıçan modelinde farklı beyin bölgelerinde [Bcl-2]/[Bax] oranını araştırmayı amaçlıyoruz.Metod: Dişi Sprague-Dawley sıçanlar ters 12 s aydınlık/karanlık siklusunda 10 dak. kirli kedi kumuna maruz bırakıldı ve protokol 1 hafta sonra travma çağrıştırıcı (temiz kum) ile tekrarlandı. Sıçanlara intraperitonel tuzlu su, fluoksetin (2.5 mg/kg/day) veya propronolol (10 mg/kg/gün) uygulama dönemleri arasında 7 gün verildi. Travma çağrıştırıcıya maruz bırakmanın ardından yükseltilmiş artı labirent yapıldı. Western blot dorsal hipokampus, frontal korteks ve amigdalar bölge homojenatlarında Bcl-2 ve Bax proteinlerinin miktarını belirlemede kullanıldı.Bulgular: Fluoksetin, ankisiyete indeksleri ve dona kalma sürelerindeki artışları geri çevirdi. Amigdalar bölgede ve frontal korteks de [Bcl-2]/[Bax] oranı travmatik kontrol sıçanlarda anlamlı olarak azaldı (p<0.0001), fakat dorsal hipokampusda azalmadı. Fluoksetin apoptotik değişimleri geri çevirmesine rağmen propranolol çevirmedi ve proapoptotik proteinde artışa sebep oldu. Sonuç: Bu sonuçlarla fluoksetinin nöroprotektif rolü önerilebilir fakat propranolol için önerilemez
The B-cell lymphoma/leukemia-2 (Bcl-2) family of proteins governs mitochondrial membrane permeability where the programmed apoptotic process is controlled by the balance between proapoptotic (Bax) and antiapoptotic (Bcl-2) proteins. We aimed to investigate the [Bcl-2]/[Bax] in different brain regions in a post-traumatic stress disorder rat model.Methods: Female Sprague-Dawley rats were exposed to dirty cat litter (trauma) for 10 min and the protocol was repeated 1 week later with a trauma reminder (clean litter) in reversed 12 h light/dark cycle. The rats received intraperitoneal saline, fluoxetine (2.5 mg/kg/day) or propranolol (10 mg/kg/day) for 7 days between exposure sessions. Following exposure to the trauma reminder, elevated plus maze experiments were done. Immunoblotting was used to quantify [Bcl-2] and [Bax] proteins in the homogenates of the dorsal hippocampus, the frontal cortex and the amygdaloid complex.Results: Fluoxetine reversed the increases in the anxiety indices and the freezing times. In the amygdaloid complex and the frontal cortex, the [Bcl-2]/[Bax] decreased in the traumatized control rats significantly (p<0.0001), but not in the dorsal hippocampus. Although the fluoxetine treatment reversed the apoptotic changes but propranolol failed and caused proapoptotic proteins to increase.Conclusion: These results may suggest a neuroprotective role for fluoxetine but not for propranolol
The B-cell lymphoma/leukemia-2 (Bcl-2) family of proteins governs mitochondrial membrane permeability where the programmed apoptotic process is controlled by the balance between proapoptotic (Bax) and antiapoptotic (Bcl-2) proteins. We aimed to investigate the [Bcl-2]/[Bax] in different brain regions in a post-traumatic stress disorder rat model.Methods: Female Sprague-Dawley rats were exposed to dirty cat litter (trauma) for 10 min and the protocol was repeated 1 week later with a trauma reminder (clean litter) in reversed 12 h light/dark cycle. The rats received intraperitoneal saline, fluoxetine (2.5 mg/kg/day) or propranolol (10 mg/kg/day) for 7 days between exposure sessions. Following exposure to the trauma reminder, elevated plus maze experiments were done. Immunoblotting was used to quantify [Bcl-2] and [Bax] proteins in the homogenates of the dorsal hippocampus, the frontal cortex and the amygdaloid complex.Results: Fluoxetine reversed the increases in the anxiety indices and the freezing times. In the amygdaloid complex and the frontal cortex, the [Bcl-2]/[Bax] decreased in the traumatized control rats significantly (p<0.0001), but not in the dorsal hippocampus. Although the fluoxetine treatment reversed the apoptotic changes but propranolol failed and caused proapoptotic proteins to increase.Conclusion: These results may suggest a neuroprotective role for fluoxetine but not for propranolol